DESCRIPTION: The "stress-illness" relationship is not a linear and invariant relationship due to a multitude of factors including genetic background, gender, health behaviors, developmental experiences, and many as yet unidentified characteristics of the individual. Therefore, the lack of uniform agreement regarding the role of emotions and behavior in modulating the activity of the immune system is not surprising. Unquestionably, physiological homeostasis is affected by a host of intervening variables. Rate of progression to Acquired Immunodeficiency Syndrome (AIDS) after exposure to human immunodeficiency virus (HIV) can be quite variable with few, if any, explanations. Even among long-term survivors of HIV, there remains considerable heterogeneity in their characteristics even after accounting for genetic contributions. Post-infection predictors of progression in HIV have been identified but pre-infection predictors are limited. Early rearing experiences have profound effects on the responsivity of the hypothalamic-pituitary-adrenal axis (HPA). These experiences can create an organism at greater or lesser risk for activation of the HPA system. Components of the HPA system, namely cortisol (CORT) and dihydroepiandrosterone (DHEA) affect regulation of the immune system and alter viral susceptibility. Specifically DHEA acts as a regulatory brake on the immunosuppressive effects of CORT. These steroids affect the balance in immune regulatory substances, the Type 1 (IL-2, IL-12, TNF-alpha, and INF-gamma) and Type 2 (IL-4, IL-6, and IL-10) cytokines, with consequences for viral defense in immunodeficiency. In spite of the availability of many prognostic indicators postinfection, there remain few, if any, indicators that reliably predict outcome prior to infection. Knowledge of preexisting conditions setting the stage for rapid progression post-infection is an important goal for AIDS research. The present application seeks to identify developmental factors affecting the HPA axis and the balance of CORT and DHEA with consequences for individual differences in rates of progression in immunodeficiency disease.